A significant problem for biomedicine generally and mental health specifically is understanding how individual variation in phenotype is produced. In this proposal we continue our previous approach of attempting to generalize the dominant model of sexual differentiation, the organizational-activational model, to an understanding of the neuroendocrine mechanisms that produce individual variation in aggressive behavior. For these studies we use a nontraditional model, an animal with alternative male phenotypes or morphs. The morphs differ in color and one morph is highly aggressive, while the other is not. This model system is powerful because we can use color to assign individuals to behavioral phenotypes that differ in only one dimension, aggressiveness. In previous funding periods, we learned that differences in behavior between these morphs are organized by early actions of sex steroid hormones in a manner analogous to the organization of sexual phenotype. This result suggests that differences within the sexes may be produced by mechanisms very similar to those that produce differences between the sexes. We propose here to examine this effect more closely and to focus on a more detailed level of the specific mechanisms within the brain. Where do these hormones act in the brain and how does this change during the course of development? What neuroanatomical and neurochemical changes do these hormones produce to bring about the differences in aggressive behavior? How does experience modify the effects of these hormones on these neural substrates? We also propose to test a working hypothesis, the Dual Gate Hypothesis, that is a specific extension of the organizational-activational model and that proposes that the differences in behavior are produced by the early actions of hormones on at least two specific areas of the brain, the medial amygdala and the periventricular nucleus of the hypothalamus.